This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ayers, J. I.
Right arrow Articles by Bartz, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ayers, J. I.
Right arrow Articles by Bartz, J. C.

 Previous Article  |  Next Article 

Journal of Virology, January 2009, p. 81-87, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01745-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Prion Strain Targeting Independent of Strain-Specific Neuronal Tropism{triangledown}

Jacob I. Ayers,1 Anthony E. Kincaid,1,2 and Jason C. Bartz1*

Departments of Medical Microbiology and Immunology,1 Physical Therapy, Creighton University, Omaha, Nebraska 681782

Received 18 August 2008/ Accepted 17 October 2008

While neuropathological features that define prion strains include spongiform degeneration and deposition patterns of PrPSc, the underlying mechanism for the strain-specific differences in PrPSc targeting is not known. To investigate prion strain targeting, we inoculated hamsters in the sciatic nerve with either the hyper (HY) or drowsy (DY) strain of the transmissible mink encephalopathy (TME) agent. Both TME strains were initially retrogradely transported in the central nervous system (CNS) exclusively by four descending motor tracts. The locations of HY and DY PrPSc deposition were identical throughout the majority of the incubation period. However, differences in PrPSc deposition between these strains were observed upon development of clinical disease. The differences observed were unlikely to be due to strain-specific neuronal tropism, since comparison of PrPSc deposition patterns by different routes of infection indicated that all brain areas were susceptible to prion infection by both TME strains. These findings suggest that prion transport and differential susceptibility to prion infection are not solely responsible for prion strain targeting. The data suggest that differences in PrPSc distribution between strains during clinical disease are due to differences in the length of time that PrPSc has to spread in the CNS before the host succumbs to disease.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, 2500 California Plaza, Omaha, Nebraska 68178. Phone: (402) 280-1811. Fax: (402) 280-1875. E-mail: jbartz{at}creighton.edu

{triangledown} Published ahead of print on 29 October 2008.

Journal of Virology, January 2009, p. 81-87, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01745-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Piro, J. R., Harris, B. T., Nishina, K., Soto, C., Morales, R., Rees, J. R., Supattapone, S. (2009). Prion Protein Glycosylation Is Not Required for Strain-Specific Neurotropism. J. Virol. 83: 5321-5328 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»